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BULLETIN OF THE 

u. 

No. 65 

Contribution from the Bureau of Animal Industry, A. D. Melvin, Chief 
February 14, 19 1 4. 

(PROFESSIONAL PAPER.) 

CEREBROSPINAL MENINGITIS ("FORAGE 
POISONING"). 

By John R. Mohler, Y. M. D., Chief of the Pathological Division. 
INTRODUCTION. 

About 100 3'Oars ago (1813) there appeared in Wurttemberg a fatal 
disease of horses which was termed "head disease" owing to the pro- 
nounced manifestation of brain symptoms. The affection spread 
through certain sections of Europe from 1824 to 1828 and was de- 
scribed as "fever of the nerves." In 1878 the attention of the veter- 
inarians of Saxony was attracted to the disease, which was then 
termed "nervous siclaiess," and within the next 10 years it assumed 
an epizootic character. In fact the malady became so prevalent in 
and around Borna (near Leipsic, Germany) during the nineties that 
it became Imown as the Borna disease. The affection has spread like 
a plague on two occasions in Belgium, and has also exacted a heavy 
toU in Russia, Great Britain, Austria-IIungaiy, and elsewhere. Its 
appearance in America is by no means of recent occurrence, for the 
malady was reported by Large in 1847, by Michener in 1850, and by 
Liautard in 1869 as appearing in both sporadic and enzootic form in 
several of the Eastern States. Since then the disease has occurred 
periodically in many States in all sections of the countr}^, and has been 
the subject of numerous investigations and publications by a number 
of the leading men of the veterinary profession. It is prevalent with 
more or less severity every year in certain parts of the United States, 
and durmg the year 1912 the Bureau of Animal Industry received 
urgent requests for help from Colorado, Georgia, Iowa, Kansas, Ken- 
tucky, Louisiana, Maryland, Missom-i, Nebraska, New Jersey, North 
Carolina, Oregon, South Carolina, South Dakota, Virginia, and West 
Virginia. While in 1912 the brunt of the disease seemed to fall on 
Kansas and Nebraska, other States were also seriously afflicted. 
In previous years, for instance in 1882 as well as in 1897, the horses of 
southeastern Texas were reported to have died by the thousand, and 

Note. — This publication gives information about a serious disease of horses; it is especially suited to 
veterinarians in the States west of the Mississippi River and in the South. 

22575°-i4 jyionograph 



BULLETIN 65, U. S. DEPARTMENT OF AGRICULTURE. 






q,<('^M> 



in the following year the horses of Iowa were said to have ''died like 
rats." However, Kansas seems to have had more than her share of 
this trouble, as a severe outbreak that extended over almost the entire 
State occurred in 1891, while in 1902 and again in 1906 the disease 
recurred with equal severity in various portions of the State. 

NOMENCLATURE. 

There has always been considerable discussion and criticism re- 
garding the different names which have been given this malady, and 
various terms have been apphed according as each author in past 
outbreaks has considered certain symptoms or lesions as the para- 
mount feature of the affection. Thus the disease has been termed 
"cramp of the neck," ''head disease," "mad staggers," "sleepy staggers," 
etc. Through the recent investigations of Grimm, Schmidt, and others 
it has been quite definitely established that "head disease," Borna 
disease, and cerebrospinal m.eningitis are one and the same, and 
Hutyra and Marek have accepted this opinion and incorporated it 
in their "Special Pathology." While at first the Borna disease was 
considered as a form of cerebrospinal meningitis, the work of Johne 
and Ostertag (1900) indicated that it was an independent disease, 
because they failed to find any inflammatory changes in the central 
nervous system. Accepting this view, Friedberger and Frohner 
have separated the two diseases in their "Theory and Practice," 
basing their dift'erential diagnosis chiefly on the absence of inflam- 
mation in the brain and cord of Borna disease. However, since the 
publication of this excellent work in 1904, Oppenheim, Dexler, 
Schmidt, and others hav^e shown conclusively that inflammatory 
lesions are present in the central nervous system, although Dexler 
has pointed out that in s(nne cases it is necessary to make a sys- 
tematic examination of a number of shdes to discover the inflamma- 
tory changes. As a result the more recent WTiters have adopted 
the viewpoint that the two terms, Borna disease and cerebrospmal 
meningitis, are synonymous. 

When this disease appeared with such severity in certain sections 
of the United States in the summer of 1912, there were a number of 
persons who claimed that it was the Borna disease appearing in the 
New World for the first time ; others diagnosed it as a new horse 
disease, as influenza, parasitism (due to the palisade worm), paralysis 
sunilar to poliomyelitis (infantile paralysis) of man, epidemic cerebro- 
spmal meningitis of man, and equine malaria from the fact that 
mosquitoes were prevalent and the horses were in lowlands. These 
erroneous diagnoses, while particij)ated in to a certain extent by 
some veterinarians, were usually the opinions of physicians, chem- 
ists, bacteriologists who were not veterinarians, and others of Umited 
veterinary experience. However, the vast majority of veterinary 

a OF D. 
H^M 2 1914 



CEREBROSPINAL MENINGITIS (" FORAGE POISONING "). 3 

practitioners recognized the disease as their okl torment — cerebro- 
spinal meningitis, staggers, or forage poisoning. 

The latter name came into the hterature of the disease as a 
synonym m 1900 following the mvestigation of an outbreak by 
Pearson. He was able to reproduce the disease in experiment 
horses by feeding them on damaged silage, and by giving them 
water to drink wliich had percolated through this silage. Doubtless 
influenced by the frequent absence of microscopic lesions of the 
central nervous system, and by the analogy between this disease 
and meat poisoning of man, Pearson proposed the name forage 
poisoning, wliich has been more or less in favor ever since. There 
are certain objections to this term, principally from the fact that it 
may suggest a form of poisoning produced by vegetation that is 
specifically poisonous, such as lupines, loco, larkspur, etc., or by 
ordinary forage that is poisonous of itself. This, however, was not 
the intention of Pearson, for by his analogy to meat poisoning it is 
evident that he did not wish to convey the mipression that all forage 
was poisonous any more than all meat is poisonous. But when 
meat becomes contammated with pathogenic bacteria, such as the 
Bacillus enteritidis, B. hotulinis, etc., such meat is (hmgerous to 
man in the same mamier that ordinary forage contaminated with 
certain unknown infective agents becomes dangerous to horses and 
produces forage poisonmg. In other words, the forage is the carrier 
and not the primary factor in the disease. On the other hand, 
tliis term has a direct advantage in being readily understood in 
popular usage and in conveying to the layman's mind that an 
absolute change in feed is essential. 

After years of study and experimentation it is the consensus of 
opinion of practically all investigators that the disease can be con- 
trolled efi^ectively only by a total change of feed and forage; in other 
words, by preventive measures and not by medicmal treatment. 
That there is direct connection between ingestion of green forage, 
exposed pasturage, newl}^ cut hay and fodder, and the development 
of the disease is quite ob\dous, and that the ingestion of such forage 
when contaminated is the most important factor is equally obvious, 
as almost 100 per cent of the cases in Kansas and over 95 per cent 
of the cases in Nebraska of which we have any record were maintained 
all or part of the time under such conditions. Even such negative 
history is not always dependable, as the owner on one farm informed 
the writer positively that the dead horses had eaten nothing except 
old hay and grain, but when notice was taken of the closely cropped 
grass in an adjacent pasture he innocently remarked that he always 
turned the work horses into the pasture over night. In fact in some 
sections "pasture disease" is the designation for this malady. 



4 BULLETIN 65, U. S. DEPARTMENT OF AGRICULTURE. 

Other names which have been given to this affection are epizootic 
encephalo-myelitis, merdngo-encephahtis and ineningo-myeHtis, en- 
zootic cerebritis, leuco-encephalitis, etc., but the writer prefers the 
old-fashioned terms cerebrospinal meningitis for the scientific term 
and "blind staggers" for the lay term. That the symptom of stag- 
gering is one of the most common mainfestations of the disease is 
shown by the clinical observations of Schmidt, who has made a close 
study of 415 cases, 377 of which developed staggering symptoms 
while standing or walking. The only symptom which occurred more 
frequently was the loss of appetite appearing in 410 animals, while 
the symptoms next in prominence were grinding of the teeth, which 
was observed in 349 cases, and difficulty in sw^allowing, which occurred 

in 335 cases. 

ETIOLOGY. 

Unfortunately no specific bacteria, fungus, virus, or other toxic 
principle has yet been found which can be considered as the cause 
of cerebrospinal meningitis in the horse. It is quite true that bac- 
teriological investigation has given us a number of different organ- 
isms by an equal number of different investigators, each of whom 
has thought his particular organism to be the causative agent of the 
disease; but the fact remains that the four rules laid down by Koch 
have not been met with sufficient regularity to make the results 
satisfactory to the disinterested worker. Further investigations are 
necessary to decide wliich, if any, of the reported organisms is the 
ti'ue cause of the disease. That the disease may not have an etio- 
logical entity has been suggested by Weichselbaum, Hutyra, and 
Marek. This would seem cjuite probable if all the claims for the 
following different etiological factors were to be accepted. For 
instance, Siedamgrotsky and Schlegel incriminated a micrococcus as 
the cause of the disease. On the other hand, Johne found diplococci 
in the cerebrospinal fluid which he termed Diplococcus intracellularis 
equi. Again, Ostertag recovered streptococci in short chains from 
the blood, liver, urine, and brain of affected horses. These organ- 
isms he termed Borna streptococci. Harrison of Canada isolated a 
streptococcus from the brains of horses affected with cerebrospinal 
meningitis which was quite similar to Ostertag 's, although it differed 
in forming capsules, staining by Gram's method, refusing to grow 
well on gelatin, and in proving virulent for laboratory animals. In 
Minnesota, Wilson and Brimhall have also incriminated a diplococcus 
as the cause of cerebrospinal meningitis of horses, cattle, sheep, and 
pigs, and proved it to be the Diplococcus imeuTnonise, of Frankel. 
They likewise claimed to have isolated the Micrococcus intracellularis 
meningitidis of Weichselbaum from the central nervous system of a 
cow shoAving symptoms of spinal meningitis. Tliis latter organism 



CEREBEOSPINAL MENINGITIS ('' FORAGE POISONING"). 5 

is also reported to have been found by Christiana in primary sporadic 
meningitis in the horse and in a goat. 

The remarkable part of all the above investigations is that each 
author considers his particular organism as the etiological factor of 
the disease, and the majority of these writers behevc they have suc- 
ceeded in producing the disease in horses by the inoculation of these 
differing agents. Some of these positive results are readily explained 
by the large quantity of turbid fluid injected under the dura. The 
inoculation of 5 and 10 c. c. doses of a heavy emulsion of any organism 
is likely to produce an irritation, and the inflammation set up by 
such foreign material will necessarily produce exudation with ac- 
companying mechanical pressure, so that it is not surprising to read 
in the post-mortem notes of some of these cases that the meninges 
bulged through the opening on cutting through the bones of the skull. 

Schmidt, of Dresden, is of the opinion that the nature of the infec- 
tious principle is not settled, and believes that the cocci and dip- 
lococci which have been described as causative factors will in future 
be deprived of their pathogenic relationship. 

In two outbreaks of forage poisoning investigated by Moore, of 
Cornell, one gave negative results from a bacteriological standpoint, 
while in the other pure cultures of the colon bacillus were obtained 
from the brain. 

Grimm, working in Zwick's laboratory in Berlin, isolated strepto- 
cocci from horses affected with head disease or staggers, which were 
not essentially different from the Borna streptococci of Ostertag. 
Owing to the regularity with which these cocci were taken from the 
brains of horses with ''head disease" — cocci which Grimm stated 
possessed slight, if any, properties necessary to make them causal 
factors of disease — the question arose whether the same microorgan- 
isms are not also found in the brains of healthy horses. Grimm ob- 
tained the heads of 10 horses which were killed at the Zoological 
Garden for the animals, and which were by examination found to be 
free from any indication of cerebrospinal menhigitis. In the brains 
of these healthy horses he found cocci (staphylococci and strepto- 
cocci), although cultures were made within a few hours after death, 
and at least one strain has shown many similarities to the streptococcus" 
found by Ostertag. 

These results of Grimm's work are very similar to the results of the 
Bureau of Animal Industry. In horses which have died of forage 
poisoning it is not a difficult task to recover various forms of cocci; in 
fact, too manj^ forms to make them all of etiological significance, while 
in those cases which have been killed in the late stages of the disease 
it is of common occurrence to have all the culture media inoculated 
with the various tissues remain sterile. On the other hand, we found 
micrococci, diplococci, streptococci, and staphylococci so frequently 



6 BULLETIN 65, U. S. DEPARTMENT OP AGEICULTURE. 

ill the brains of horses which have died of dourine, swamp fever, influ- 
enza, etc., that we have come to consider these organisms as repre- 
senting an agonal invasion from the intestines without causal con- 
nection with any definite disease. Like Grimm, we have found some 
of these same cocci in the brains of horses that died of forage poison- 
ing, and we have also recovered other species, all of which have been 
inoculated into experiment horses by various methods, including 
intravenous, subcutaneous, subdural, and intralumbar injection, as 
well as by spi'aying the nasal mucous membrane, with the result that 
two horses died following a nasal douche and a subdural injection, 
resjiectively, of a pure culture of two different cocci. The post- 
mortem on the former showed death to have been due to a strangu- 
lated intestine, while the second animal died suddenly without evinc- 
ing any characteristic symptoms, although extremely nervous. Post- 
mortem examination showed an absence of any pathological lesions 
posterior to the brain. The dura mater was inflamed and distended 
"with a yellowish exudate. The veins and capillaries of the cerebrum 
were dilated and engorged with blood, while the third ventricle con- 
tained a tumor the size of a wahiut. Although the same organism which 
was injected was recovered from the brain tissue, other horses injected 
with the recovered culture have continued to remain in a healthy 
condition. 

With the view of obtaining additional information regarcUng the 
significance of these various cocci to the disease in question, an 
antigen was prepared from a culture of each organism and tested 
asramst the blood serum obtained from affected horses in the field 
for complement fiji;ation and agglutination as in glanders. In no 
case was a positive reaction to these tests obtained by the use of any 
of the antigens prepared from the diflferent cocci isolated from dis- 
eased horses. In this connection it may be noted that from the 
number of affections of the horse produced by coccoid organisms, 
this animal appears to be particularly susceptible to their action. 

Another cause has been suggested for this disease in the finding 
of nuclear inclusions by Joest and Degen in the nerve cells of the 
liippocampus. These inclusions are similar to the Negri bodies of 
rabies, and are rounded or oval in shape, staining intensely with 
eosin. A large number of brains from affected horses have been 
examined in our laboratory for these bodies, but thus far with nega- 
tive results, although the same technique apphed to the brains of 
rabid animals brings out the Negri bodies with great clearness. 

There remains one widely accepted theory as to the causation of 
the disease which must be given consideration, namely, fungi on 
the feed. Wliile most investigators have obtained negative results 
when feeding experiment animals upon moldy feed, some few have 
reproduced the disease by such feeding. Thus, Mayo reports that a 



CEKEBEOSPINAL MENINGITIS (" FOEAGE POISONING"). 7 

colt fed experimentally upon some of the moldy corn, which was 
held responsible for the serious outbreak in Kansas in 1890, developed 
the disease and died on the twenty-sixth day. Agam, the Kansas 
outbreak of 1906 was said by Haslam to have been produced by 
immature ears of corn mfected by molds, although the exact mold 
was not discovered. By feeding horses upon this immature corn 
badly infected with molds, typical fatal cases of staggers were pro- 
duced m four out of seven horses. Haslam also records the fact 
that severe losses of horses have occurred in other States when the 
grasses m the pastures became moldy. Klimmer, commentmg upon 
the negative results obtamed in experiments with moldy feed, asserts 
that the numerous losses occurring from the feeding of such material 
mdicates the probability that the experiments were not sufficiently 
extensive from which to draw conclusions, and beUeves that the use 
of such feed should be discouraged. Among other writers who have 
attributed the disease to toxic fungi are Michener, Trumbower, and 
Harbaugh. The latter investigated the serious outbreak of this 
disease which occurred in Virginia and North Carolina in 1886, and 
claimed that every case of the disease could be traced directly to 
moldy feed. 

This theory of toxic fungi is not antagonistic to the facts in many 
of the best observed outbreaks, and knowmg that fungi vary greatly 
in growth and in the elimination of various products under different 
climatic conditions, we may explain the irregularity of the symptoms 
as well as the occurrence of the disease under what may appear* to be 
identical conditions. Thus Ceni of Italy states that molds are capable 
of producing poisons, but only at certain stages of their growth, and 
at other tunes they are entirely inactive. A case of this character 
was investigated by this bureau several years ago in an outbreak 
among the United States Army horses at an encampment in Penn- 
sylvania. Many horses had died of cerebrospinal meningitis as a 
result of eatmg moldy baled hay, and as soon as the hay was elimi- 
nated the deaths ceased. Other horses in the vicmity not fed upon 
this hay failed to contract the disease. At the suggestion of State 
Veteiinarian Marshall the bales were opened and exposed to the sun 
for three or four weeks, after which tune this hay was fed sparingly 
at first and later in usual quantities without producing any ill effect. 
Forage poisoning therefore seems to be an auto-intoxication rather 
than an infection, and due to certain chemical poisons or toxins 
formed b}'- organismal activity. These toxins may be present when 
the forage is taken into the body or formed in the gastro-intestinal 
canal, and, therefore, the disease is a specific form of auto- intoxication. 
The nature of the substance which causes these harmful changes or 
the poisonous bodies that are formed remain unknown. 



8 BULLETIN 65, U. S. DEPAETMENT OF AGRICULTURE. 

On account of this very old and very plausible theory so often 
advanced, that the disease is due to toxic substances existing in 
damaged grain and fodder, a number of species of fungi were isolated 
during the past yeai from damaged corn and forage and grown on a 
sterilized corn medium or alfalfa infusion in an effort to produce some 
toxic substance that would create disease when fed to horses. The 
pure cultures were allowed to grow for periods of one month's dura- 
tion, in flasks containmg 250 cubic centimeters of the nutrient 
medium, and the contents of one flask were fed each day for periods 
of 30 days, along with a sufficient quantity of sound corn and hay to 
make a normal ration; but no symptoms have thus far developed 
in the experiment animals, although only about one-h^lf of the number 
of pure cultures isolated have thus far been used in this experiment. 

It is possible that laboratory conditions alone can not l)e made to 
parallel sufficiently close those which exist naturally in the growing 
plants, and that toxic substances which might be produced in a 
natural state would not be generated in a corn-meal medium in the 
laboratory. The by-products of the growth of both fungi and bacteria 
on corn and forage should certainly receive more consideration in 
future work. In view of the above information it must appear to 
the unbiased mind that the cause of forage poisoning remains an 
obscure and puzzling problem. 

OCCURRENCE. 

Like cerebrospinal meningitis of man, forage poisoning occurs in 
sporadic as well as enzootic and epizootic forms. The sporadic 
cases occur either in different localities from the epizootic out- 
breaks or in such sparse numbers as not to amount to an enzootic. 
Thus the outbreaks are quite variable in extent and severity. Some- 
times they become very Avidespread, causing heavy losses, as in the 
recent outbreak in Kansas and Nebraska, while at other times there 
are only sporadic cases. Liebener beheves that the development of 
the cause of the disease in Germany is favored by the rainfalls and 
warmth of the earth during summer and autumn. No conclusive 
evidence has ever been presented to indicate that the disease is ever 
transmitted directly from one horse to another. Sick animals have 
been placed alongside of susceptible horses in the same stable without 
conveying the disease to the latter, and healthy horses have been 
placed in stalls previously occupied by animals which died of the 
disease, and have eaten from the same mangers mthout previous 
disinfection, but in no case has the disease been transmitted in this 
manner. In the recent outbreak in Kansas it was quite noticeable 
that livery and other work horses were not affected so long as they 
were fed on clean, dry forage, although they were constantly exposed 



CEEEBKOSPIlSrAL MENINGITIS ('' FORAGE POISONING"). 9 

to the disease by coming in contact with diseased horses. For 
instance, Dr. Herman Busman, who was in charge of the Kansas field 
force of veterinarians of the Bureau of Animal Industry, reports a 
case where horses were kept in adjoining corrals separated only by a 
wire fence. Those on one side were fed on green forage and recently 
cut cane, and died from the disease, while those on the other side 
were fed dry feed and not one became sick. He also reports a similar 
occurrence in a livery barn where the horses had been fed on clean, 
dry feed without sickness, but when fresh cut bottom-land hay was 
substituted for the former feed the horses became sick within a few 
days. Another similar instance was reported by Dr. E. T. Davison, 
in charge of the bureau's field force in Nebraska, in the case of a 
farmer who owned a work team that was strictly barn fed. ^^Tiile 
attending the State Fair at Lincoln these horses were turned out on 
pasture for two days and both horses came down with the disease 
on the fourth and fifth days, respectively, after being taken off the 
pasture. 

It is such cases as these that have incriminated the forage and 
caused the disease to be known as ' ' pasture disease " in some locaUties. 
Indeed some veterinarians report that all the animals affected had 
been on pasture, or, having been removed from pasture, had been fed 
on recent cuttmgs of alfalfa, prairie hay, cane, or kafir corn, while no 
cases came mider observation where the animals had been on dry feed 
all summer. 

A long period of dry weather followed by rainfall with considerable 
humidity and heat seems to favor the development and dissemination 
of the disease. The period from August 1 to October 1, 1912, pre- 
sented exceptional climatic conditions in western Kansas and south- 
ern Nebraska, and it was observed that crops cut and cured before 
this date could be fed with impimity. During the first week in 
August a heavy rainfall started in Kansas and nearly twice the usual 
amount was recorded, falling mostly during the night and soaking in. 
This was followed by very high temperatures, the 17 days from 
August 23 to September 9 being the hottest series of days on record 
in Dodge City. There were also more than the usual number of 
cloudy or partly cloudy days with high relative humidities. The 
dew point was reached early at night and the deposit of dew was 
abundant, which is imcommon in that section. High humidities 
certainly continued throughout the day among the grasses near the 
soil. These grasses, which usually cure into hay on the root, became 
dotted with both parasitic and saprophytic fmigi. Water holes, 
draws, and buffalo wallows remained filled with water throughout 
most of the period. During the latter part of September frosts 
occurred, accompanied not only by cooler weather but with lower 



10 BULLETIN 65, U. S. DEPARTMENT OF AGPJCULTUEE. 

liumidity, which are the significant factors in the subsidence of the 
disease, and after the first week in October the disease practically 
disappeared. Since then many owners have placed their horses back 
on the same pastures used during the serious stages of the disease and 
there has been no ill effect noted. This would indicate that there 
are good reasons to believe the forage is no longer in condition to 
produce the disease and hence its use is safe, as in the case of the 
Pennsylvania baled hay previously mentioned. 

Somewhat similar conditions of climate obtained in Nebraska dur- 
ing the prevalence of the disease, but on September 25 a killing frost 
was recorded, followed by several light frosts and a reduction in the 
relative humidity. After this time the disease rapidly subsided and 
finally disappeared. There is not much question that some of this 
infected forage has been baled and shipped to various points, and it is 
therefore not unlikely that sporadic cases of the disease will appear 
in these sections under favorable climatic conditions. 

In this connection, attention should be called to the marked preva- 
lence last summer and fall of the disease of cattle known as mycotic 
stomatitis, which sunulates the foot-and-mouth disease of Europe 
and is caused also by contaminated forage. This disease first 
appeared in Florida and spread over Georgia, North and South Caro- 
Ima, Tennessee, Kentucky, Virginia, Maryland, and into Pennsyl- 
vania. The climatic conditions were evidently appropriate for the 
development of the causative agent on forage, and as soon as the 
animals were brought out of the pastures and stall fed, the disease 
immediately subsided. 

SYMPTOMS AND LESIONS. 

In most of the cases disturbance of the appetite, depression, and 
weakness are the first manifestations observed, although all the 
sjnnptoms vary within wide limits. 

Very soon the characteristic symptoms of the disease appear. 
There is trouble in swallowing, drooping of the head and sleepmess, 
which may give way to excitement and attacks of vertigo. An 
impairment of vision is noted, with loss of coordmation, resultmg in a 
staggermg gait or reeling while standmg. There is muscular twitch- 
ing, cramp of certain muscles, chiefly of the neck and flanks, and 
grinding of the teeth. Sometmies colicky pains are noted. If in an 
open space, the animal will walk in a circle, sometimes to the right, 
at other times to the left, and will try to push through any obstacle 
with which he comes in contact. In the stable he will press his head 
against the stall or rest it on the manger. Sometimes he will crowd 
backward or sidewise until he gets in a corner and remains there. 
If the temperature is taken at the beginning of the disease it will be 



CEKEBROSPINAL MENINGITIS ('' FORAGE POISONING"). 11 

found to be from 103° to 107° F., but within 24 hours the temperature 
gradually falls until it reaches normal and then becomes subnormal. 
The pulse is from 40 to 90 and weak, while the respirations are fluc- 
tuatmg from normal to as high as 48 per minute. There may or may 
not be drooling of saliva, depending on the extent of the paralysis 
of the pharynx. The anmial is often down on the second or third 
day and may or may not get up when urged to do so. ^Vliile down 
he will go through automatic-like movements of pacing or walking, 
resulting in acceleration of the pulse and respiration. At this time 
the legs are held out stiffly and parallel to the ground. The hmd legs 
of many of these anmials that have gone down are paralyzed and there 
is loss of sensation of the skin of these parts. The expired aii- is 
extremely fetid, and there may be a croupous-like deposit of the 
throat, which has caused the name ''putrid sore throat." The con- 
junctiva may show injected blood vessels or petechise on a yellowish- 
tmted background. Coma or somnolence may be marked in ani- 
mals going down within the first few days. Those which remain 
standmg may become yiolent or delirious, but orduiarily the horse is 
tractable and easily managed. Death usually occurs in from 4 to 8 
days, although in the acute form death may follow within 10 or 12 
hours after the first symptoms are observed, while in chronic 
cases the disease may last 2 or 3 weeks. The prognosis is very 
unfavorable, as 85 to 90 per cent of the affected anmials die, in the 
beginning of the outbreak, but later the cases become milder with a 
consequent drop in the mortality. 

On post-mortem the amount of lesions observable to the naked 
eye is in marked contrast to the severit}^ of the symptoms noted. 
The pharyiLx and larynx are mflamed in many cases, and sometimes 
coated with a yellowdsh white glutmous deposit, extending at times 
over the tongue and occasionally a little way down the trachea. The 
lungs are normal, exce])t from complications following drenching or 
recumbence for a long period. The heart is usually normal in appear- 
ance, except an occasional cluster of j)etechi[e on the epicardium, 
while the blood is dark and firmly coagulated. The mucosa of the 
stomach indicates a subacute gastritis, while occasionally an erosion 
is noted. An edematous, gelatinous mfiltration is observed in the 
subnuu'osa of such cases. The first few inches of the small intestines 
likewise may show slight mflammation hi ((^rlaui cases, while hi others 
it is quite severe; otherwise the digesti\e h-act a])])ears normal, 
excluding the presence of varying numbers of hots, Slrom/ylus vul- 
gatus, and a few other nematodes. The liver is congested and 
swollen m some cases, while it appears normal hi othej's. The spleen 
is, as a rule, normal, and at times the kidneys are slightly congested. 
The bladder is often distended with dark-colored urine, and occa- 
sionally a marked cystitis has beeii observed. Tlie adipose tissue 



12 BULLETIN 65, U. S. DEPAETMENT OF AGRICULTUKE, 

throughout the carcass may show a pronounced icteric appearance 
m certain cases. On removing the bones of the skull the brain 
appears to be normal macroscopically in a few instances, but m most 
cases the veins and capillaries of the meninges of the cerebrum, cere- 
bellum, and occasionally the medulla are distinctly dilated and 
engorged, and in a few cases there are. pronounced lesions of a lepto- 
meningitis. An excessive amount of cerebrospinal fluid is present 
in most of the cases. On the floor of the lateral ventricles of several 
brains there was noted a slight softening due to hemorrhages into the 
brain substance. There is always an abundance of fluid in the sub- 
arachnoid spaces, ventricles, and at the base of the brain, usually of 
the color of diabetic lu'ine, and containing a Imiited amount of flocculi, 
but in a few cases it was slightly blood tinged. The spinal cord was 
not found involved in the few cases examined. 

A comparative microscopic examination of the brains of horses 
which died in Kansas, New Jersey, Maryland, and Virgmia this year 
with those of horses from previous outbreaks showed the same char- 
acteristic perivascular round-cell infiltration, especially in the olfac- 
tory lobe and the hippocampus. The pia mater showed an increased 
amount of comiective tissue with dense round- cell infiltration which 
extended mto the adjacent cortical portion of the cerebrum. The 
capillary blood vessels were engorged with cells and their walls were 
greatly infiltrated. Lunited areas of leucocytic infiltration and small 
hemorrhages in the brain tissue were not infrequently observed. No 
cellular inclusions in the ganglionic cells were detected after pro- 
longed examination. 

TREATMENT. 

One attack of the disease does not confer immunit}^. Horses have 
been observed which have recovered from two attacks, and still 
others that recovered from the first but died as a result of the second 
attack. 

Inasmucli as a natural immunity does not appear after an attack 
of cerebrospmal meningitis, it might be anticipated that serum of 
recovered cases would possess neither curative nor prophylactic 
qualities. Nevertheless, experiments were made along these Imes 
with serum from recovered cases, but without any positive results. 
Similar hivestigations have been conducted by others m Europe with 
precisely the same results. With the tendency of the disease to 
produce pathological lesions in the central nervous system, it seems 
scarcely imaginable that a medicmal remedy will be found to heal 
these foci, and even where recovery takes place there is likely to 
remain some considerable disturbance in the functions, as blindness, 
partial paralysis, dumbness, etc. Indeed, when the disease once 
becomes establibb.*^! in an animal, drugs seem to lose their physio- 



CEREBROSPINAL MENINGITIS ('* FORAGE POISONING"). 13 

logical action. Therefore, with all the pre\aously mentioned facts 
before us, it is evident that the first principle in the treatment of this 
disease is prevention, which consists in the exercise of proper care in 
feedmg only clean, well-cured forage and grain and pure water from 
an uncontaminated source. These measures when faithfully carried 
out check the development of adcUtional cases of the disease upon 
the affected premises. 

While medicinal treatment has proved unsatisfactory in the vast 
majority of cases, nevertheless the first indication is to clean out the 
digestive tract thoroughly, and to accompUsh this prompt measures 
must be used early m the disease. Active and concentrated reme- 
dies should be given, preferably subcutaneously or mtravenously, 
owing to the great difficulty in swalkn\dng, even in the early stage. 
Arecolm in one-half grain doses, subcutaneously, has given as much sat- 
isfaction as any other drug. After purging the animal the treatment 
is mostly symptomatic. Intestinal disinfectants, particularly calomel, 
salol, and salicylic acid, have been recommended, and mild anti- 
septic mouth washes are advisable. Antipyretics are of doubtful 
value, as better results are obtained, if the temperature is high, by 
copious cold-water mjections. An ice pack appUed to the head is 
beneficial in case of marked psychic disturbance. One-ounce doses 
of chloral hydrate per rectum should be given if tlie patient is violent 
or muscular spasms are severe. If the temperature becomes sub- 
normal, the animal should be warmly blanketed, and if much weakness 
is shown tliis should be combated with stimulants, such as strych- 
nin, camphor, alcohol, atropin, or aromatic spirits of amnionia. 
Early in the disease urotropin (hexamethylenamin) in doses of 25 
gi'ains, dissolved in water and given by the mouth every two hours, 
appeared to have been responsible for the recovery of some cases of 
the malady. During convalescence the usual tonic treatment is 
indicated. 

Many of the so-called "cures" made their reputation at the time 
the outbreak was abating and when nonmterference was proved to 
be equally effective. One of the most unpleasant developments of 
the outbreak in 1912 was the great amount of "'fakhig," which 
seemed to be the onh^ contagious feature connected with the disease. 
All lands of drug specifics, serums, and vaccmes developed like mush- 
rooms and were exploited in almost every community devastated by 
the disease. Many tainted dollars were obtained from the suffering 
horse o\\^lers, who gras])ed at every newly advanced treatment like 
drowning men clutcliing at straws. In Kel)raska, blackleg vaccine 
was reported to have been used as a ])reventive on at least 1,600 horses, 
and nearly 1,500 of them are said to ha^'c died as a direct result of the 
vaccine. This featm'e is now being investigated by the Government. 



14 BULLETIN 65, U. S. DEPARTMENT OF AGRICULTURE. 

Dr. ]\lunn, of Kearney, Nebr., had apparently good success from 
the use of diphtheria antitoxui as a prophylactic agent, since not a 
single animal developed the disease out of over 500 injected. It 
may be with this treatment, as with others, that good results 
were due to the fact that the disease was on the wane before treat- 
ment was commenced, but no other hne of treatment gave as good 
apparent results. Dr. Kaupp also reports in the Breeders' Gazette 
that only 1 horse died out of 900 inoculated with a diplo-strepto- 
coccic bacterm he prepared, but the injections were made so late in 
the outbreak that its value is still problematical, since thousands of 
horses in the affected area at this period failed to develop the disease, 
although they had received no preventive treatment whatsoever. 



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